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Ellsworth C. Alvord, Jr, MD

Arch Neurol. 1976;33(2):73-75.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

Many hypotheses have been offered to explain the great rarity of extracranial metastases of gliomas and the role of the craniotomy that has almost always preceded the development of even those rare occurrences. Resistance of the endothelium to invasion by gliomas, resistance of the lungs to growth of gliomas (especially medulloblastomas), inability of gliomas to induce stroma, and immunological factors have been cited,¹ but no one seems to have seriously considered the time elements that may be involved.

The cytokinetics of neoplastic growth may be quite complicated.^2-4 An apparent decrease in the growth rate as a tumor increases in size could follow necrosis or the production of sterile end-cells decreasing the proportion of cells that are actually proliferating. An apparent increase in the growth rate could follow if the proportion of cells entering the proliferating pool increases (eg, following partial removal and internal decompression³) or if blocking . . . [Full Text PDF of this Article]

Author Affiliations
From the Department of Neuropathology, University of Washington School of Medicine, Seattle.

Footnotes
Accepted for publication March 3, 1975.

Reprint requests to RJ-05 (Neuropathology), University of Washington School of Medicine, Seattle, WA 98195 (Dr Alvord).

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